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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1994-7-13
pubmed:abstractText
This study was undertaken to investigate the effects of newly isolated T lymphotropic viruses, human herpesvirus (HHV)-6 and HHV-7, on CD4+ T cells. We first examined changes in surface molecule expression on CD4+ T cells after infection with HHV-6 or HHV-7 by flow cytometry. Among surface molecules examined, CD3 expression appeared to decline markedly after infection with HHV-6 variant A (strain U1102) but the decreased level of CD3 expression after infection with HHV-6 variant B (strain Z29) was slight. Impairment of surface CD3 expression on HHV-6 variant A-infected cells was also demonstrated by measuring intracellular free Ca2+ concentration in response to anti-CD3 mAb. In contrast, HHV-7 infection induced a marked loss of surface CD4 expression, but the decline of CD3 expression was slight. Cytotoxic activity of virus-specific CD4+ CTL clones decreased after infection with both HHV-6 variant A or HHV-7 but the degree of reduction of cytotoxicity by HHV-6 variant B was not significant. Addition of lectin restored the cytotoxicity of HHV-7-infected CTL but not that of HHV-6 variant A-infected CTL. Northern blot analysis and immunoprecipitation showed that infection with HHV-6 and HHV-7 did not affect the transcription and protein synthesis of CD3 and CD4. These findings suggest that both HHV-6 and HHV-7 may directly cause T cell immunodeficiency but that the mechanisms of CD4+ T cell dysfunction mediated by HHV-6 and HHV-7 are different.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
152
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5768-75
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Distinct effects of human herpesvirus 6 and human herpesvirus 7 on surface molecule expression and function of CD4+ T cells.
pubmed:affiliation
First Department of Internal Medicine, Ehime University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't